1. Field of the Invention
The present invention relates to cardiac pacemakers which involve cardiac stimulation in order to provide a clinically and therapeutically accepted method for correcting heart block, sick sinus node syndrome and specific other arrhythmias.
2. Description of the Prior Art
The parts of heart normally beat in an orderly sequence beginning with the contraction of the atria (atrial systole) and followed by contraction of the ventricles. During the diastole all four chambers of the heart are relaxed. The specialized structures that form the cardiac conduction, including the sino-atrial node (SA node), the atrioventricular node (AV node) the bundle of HIS followed by right and left branches and the Purkinje system, discharge at a more rapid rate than the cardiac muscle itself. The SA node normally discharges most rapidly with the depolarization spreading from it to other regions before they discharge spontaneously. Thus it can be seen that the SA node is the normal inherent cardiac pacemaker with its rate of discharge determining the rate at which the heart beats. The impulses which are generated in the sinus (SA) node pass through the atrial muscle to the AV node on its way to the ventricular muscle.
In the normal human heart, each beat originates in the sinus node with the heart beating about 70 times per minute at rest. The rate is slowed (bradycardia) during sleep and accelerated (tachycardia) by exercise, fever and many other stimuli. Abnormal variations in the heart rate are called sinus arrhythmia. A portion of the AV node sometimes discharges independently and if this occurs once, the result is a beat which occurs before the expected next normal beat and transiently interrupts the cardiac rythm. This is called either an atrial, nodal or ventricular extrasystole or premature beat. If this occurs repetitively at a rate more rapid than that of the sinus node it produces a rapid regular tachycardia. While occasional atrial extrasystoles occur from time to time in most normal elderly humans and have no clinical significance, the repetitive discharge causing atrial tachycardia and flutter resulting in ventricular rates which may indicate that the ventricular rate may be so high that diastole is too short for adequate filling of the ventricules with blood between contractions. This means that the cardiac output is reduced and symptoms of heart failure may appear.
One of the specific treatments for correcting heart block, sick sinus node syndrome and specific other arrhythmias involves "physiological stimulation" of both sets of chambers of the heart. Studies have been conducted of the so-called sequential stimulation over a wide range of stimulation parameters in connection with a study of the hemodynamic properties of the heart, as reported in an article by Samet et al, entitled "Hemodynamic Sequelae of atrial, Ventricular and Sequential Atrial Ventricular Pacing in Cardiac Patients", American Heart Journal, Vol. 72, pages 725-729, December, 1966.
Earlier than that, P-wave synchronous coupling of both chambers was found to produce substantially better antiarrhythmic properties than simple stimulation of the ventricles. As described by Nathan et al in an article entitiled "An Implantable Synchronous Pacemaker for the Long Term Correction of Complete Heart Block", American Journal of Cardiology, Vol. 11, page 362, 1963. Bradycardia have been treated with fixed rate ventricular pacing which competed with, or was out of synchronism with, the true sinus rate.
Implantable versions of AV-sequential pacemakers, as they are disclosed in U.S. Pat. No. 3,747,604 and which are based on the work reported in the above-cited article by Samet et al, provide atrial escape stimuli before ventricular escape stimuli so that the protection against arrhythmias is augmented particularly in the bradycardia modes. In this connection, the term "escape stimuli" is intended to mean that the artificial cardiac pacemaker emits a stimulation pulse unless a corresponding signal appears from the heart itself within a given interval.
Studies with an implantable Multimode A-V Pacemaker for Reciprocating Atrioventricular Tachycardias, PACE, Vol. 3, May, 1980, indicate ways in which arrhythmias can be initiated, eliminated and suppressed by suitable stimulation of one of the two chambers of the heart, even if in some patients coupling is effected in the reverse direction.
The literature on cardiac arrhythmias is replete with diagrams and listings of criteria for the "Reentry Arrhythmias" of the dominant type where two stimulation pathways must exist to maintain the arrhythmia. A reentry tachycardia is a fast heat rate caused by reentry path way providing a new cardiac cycle of activity from the previous activity. In a normal heart beat, as discussed above, the sequence of cardiac activity begins at the sinus node, proceeds via the AV node and into the right and left ventricular chambers. The electrical activity produces an atrial contraction followed by delayed ventricular contraction. The depolarization activity originating at the pacemaker cells of the sinus node is extinguished when all of the ventricular cells have depolarized. The cells cannot support further activity until they are repolarized and the new activity is initiated.
During the period when all of the cells in a group are depolarized that area of the heart is said to be in absolute refractory. When part of the cells in a group are repolarized the area is said to be in relative refractory. In a totally non-refractory area it is generally possible for activation to propagation in either direction. However, in an area of relative refractory the direction of propagation favors the area with the greater density of repolarized cells. As will be discussed later, this is one explanation for the direction of propagation tending to go in only one of two possible directions in the pathway. Another possibility is when one path is fully recovered in front of new activity while the other path has slowly recovering cells to obstruct propagation of new activity. When the activity traverses the first path and echos back along the second path it encounters fully recovered cells making continued propagation possible.
When there is only one pathway from the atria to the ventricle there can be no reentry and no restarting of cardiac activity. Thus it can be seen that one of the primary requirements for reentry tachycardia is two conducting pathways that form a closed loop where activity can propagate around the loop sustaining itself. This closed loop acts as a pacemaker where each transit around the loop provides new excitation to chambers of the heart that are linked by conductive paths to the loop. This requirement for a bifurcated pathway from the atrium to the ventricle is shown in the FIG. 1.
If the propagation time around the loop is shorter than the refractory period of cells everywhere in the loop the propagation will be stopped when the activity collides with the refractory cells. Therefore a second criteria for reentry tachycardia is that the conduction time in the loop must be relatively long compared to the refractory times throughout the loop so that at least somewhere in one of the branches there must be a relatively slow propagation of activity.
A third criteria for the reentry tachycardia to take place is that upon entry or beginning of activity, one of the conducting pathways must at least temporarily block or be refractory to excitation. This is evident from the fact that when activity enters the loop from one of the chambers and conduction takes place in both directions the activity will be extinguished when they collide on the other side of the loop. However, if upon entering the loop it propagates in only one of the two directions it will not be extinguished and it is now free to continue to conduct around the loop forming the undesirable reentry tachycardia. The FIG. 1 illustrates a path formed by a closed loop which includes no tissue from either the atria or the ventricals. There are conducting links from the closed loop to each of the two heart chambers. It is assumed in artificial electrical pacing that there is no direct access to the loop other than the access provided by the links to the heart chambers where electrodes can be located. The properties of these links determine the accessability of the loop for an arrhythmia breaking event.
A normal sinus beat is illustrated by the FIG. 2 with the darkened areas indicating a depolarization region which begins at the sinus node in the atrium and progresses down both branches of the loop, although slightly slower in the right branch. FIG. 2c illustrates the position of the activity or depolarization which occurs when the left branch or the faster branch is depolarized to the ventricle area. It should be noted that as the activity reaches the ventricle it proceeds to go up the right or slower path where it collides with the activity coming down the slower or right branch. The FIG. 2d illustrates all of the area being depolarized and the FIG. 2e indicates a recovery of the atrium with a relative refractory part shown in the lower right side of the atrium. The link from the atria to the two paths is fully recovered and repolarization of the tissues in the right and left branches progressing a shown. the dots represent pockets of late recovering cells which can be left after all other cells surrounding the pocket have recovered.
FIG. 3 indicates an example of the operation of a premature atrial stimulation systole. The activity spreads from the atrial stimulus S.sub.a before the top link of the AV path is fully recovered, as is illustrated in FIG. 3a. From that point the stimulation activity is seen to reach to the top of the loop where the two paths bifurcate, in FIG. 3b at which point in time the tissue is in relative refractory. The density of the repolarized cells to the left is higher and conductivity is favored in that direction and blocked to the right. Another possibility is that all the cells at the top of both paths could be fully recovered and the approaching activity could go in both directions with recovering cells just ahead of the activity. At that point a pocket of late recovering cells in the right path could block conduction which continues unabated in the left branch. The FIG. 3c illustrates that repolarization from the previous beat proceeds in both paths while propagation of the new early beat continues only in the left path. The FIGS. 3d and 3e illustrates the new activity reaching the bottom junction of the paths and finding non refractory cells in both directions permitting propagation both to the ventricles and back toward the atria. FIG. 3f illustrates the activation reaching the top along the fully recovered right branch where it finds the first part of the left branch sufficiently repolarized to support propagation. The final step in the reentry process is accomplished as shown in FIG. 3g which shows the looping process which will be sustained as long as the speed of propagation is slower than the recovery time (refractory) of the cells of the loop.
Thus it can be seen that the three criteria for reentry tachycardia are (1) Two pathways, (2) Relatively slow conduction somewhere in the loop and, (3) Unidirectional conduction in one of the paths. The activity continues to propagate around the loop until cardiac parameters change enough to fail to satisfy the three criteria. Each time the activation passes the top or the bottom of the loop it branches out to stimulate the respective chamber except when the link or the chamber is refractory.
The literature on cardiac arrhythmia is replete with diagrams in listing of criteria for the "reentry arrhythmia" of the dominate type where two stimulation pathways must exists to maintain the arrhythmia. It is shown that delay periods of the loop must be relatively long to meet the requirement for sustained reentry. All prior art attempts to terminate tachyarrhythmias by stimulation have the drawback that the success "in the various methods per se" is not yet satisfactory.